Abstract

INTRODUCTION. Central nervous system pathology is a recognized consequence of HIV infection. This neuropathology results in HIV-1 Associated Dementia (HAD). Reported estimates for the frequency of HAD are as high as 31%. When the frequency of HAD is correlated with age, it is found that adults (Age: 60 years and greater) present with over twice the frequency of HAD as compared to young adults (ages 20-30) (1). There has been very little neuropathologic analysis of HIV/CNS infection in senior citizens. This may be because of the low number of HIV cases in this population at the present time. However, improved therapy is resulting in patients with increased age. Significantly, current studies have shown that while HAART can control many of the symptoms of AIDS, there is still a question of its effectiveness on preventing HAD (2). These points underscore the need for study of HIV/CNS infection in the aging and long-term survivors. It also raises the question as to why this particular population has an increased risk for developing HAD. There are several hypotheses that come to mind. One is the possibility of the combined effects of aging and HIV. Other mechanisms may also be operational. By studying the postmortem brain tissue from patients with AIDS (age greater than 60) it was hoped that further insight could be gained as to why the elderly present with increased risk for HAD.

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